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Variation in SARS-CoV-2 free-living survival and environmental transmission can modulate the intensity of emerging outbreaks.

ABSTRACT: Variation in free-living, microparasite survival can have a meaningful impact on the ecological dynamics of established and emerging infectious diseases. Nevertheless, resolving the importance of environmental transmission in the ecology of epidemics remains a persistent challenge, requires accurate measuring the free-living survival of pathogens across reservoirs of various kinds, and quantifying the extent to which interaction between hosts and reservoirs generates new infections. These questions are especially salient for emerging pathogens, where sparse and noisy data can obfuscate the relative contribution of different infection routes. In this study, we develop a mechanistic, mathematical model that permits both direct (host-to-host) and indirect (environmental) transmission and then fit this model to empirical data from 17 countries affected by an emerging virus (SARS-CoV-2). From an ecological perspective, our model highlights the potential for environmental transmission to drive complex, non-linear dynamics during infectious disease outbreaks. Summarizing, we propose that fitting such models with environmental transmission to real outbreak data from SARS-CoV-2 transmission highlights that variation in environmental transmission is an underappreciated aspect of the ecology of infectious disease, and an incomplete understanding of its role has consequences for public health interventions.

SUBMITTER: Ogbunugafor CB

PROVIDER: S-EPMC7273281 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Clustering infections by genetic similarity is a popular technique for identifying potential outbreaks of infectious disease, in part because sequences are now routinely collected for clinical management of many infections. A diverse number of nonparametric clustering methods have been developed for this purpose. These methods are generally intuitive, rapid to compute, and readily scale with large data sets. However, we have found that nonparametric clustering methods can be biased towards identifying clusters of diagnosis-where individuals are sampled sooner post-infection-rather than the clusters of rapid transmission that are meant to be potential foci for public health efforts. We develop a fundamentally new approach to genetic clustering based on fitting a Markov-modulated Poisson process (MMPP), which represents the evolution of transmission rates along the tree relating different infections. We evaluated this model-based method alongside five nonparametric clustering methods using both simulated and actual HIV sequence data sets. For simulated clusters of rapid transmission, the MMPP clustering method obtained higher mean sensitivity (85%) and specificity (91%) than the nonparametric methods. When we applied these clustering methods to published sequences from a study of HIV-1 genetic clusters in Seattle, USA, we found that the MMPP method categorized about half (46%) as many individuals to clusters compared to the other methods. Furthermore, the mean internal branch lengths that approximate transmission rates were significantly shorter in clusters extracted using MMPP, but not by other methods. We determined that the computing time for the MMPP method scaled linearly with the size of trees, requiring about 30 seconds for a tree of 1,000 tips and about 20 minutes for 50,000 tips on a single computer. This new approach to genetic clustering has significant implications for the application of pathogen sequence analysis to public health, where it is critical to robustly and accurately identify clusters for the most cost-effective deployment of outbreak management and prevention resources.

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Variation in SARS-CoV-2 free-living survival and environmental transmission can modulate the intensity of emerging outbreaks.

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